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Mast cell effector mechanisms

S J Lane1, T H Lee

  • 1Department of Allergy and Respiratory Medicine, Guy's Hospital, London, United Kingdom.

The Journal of Allergy and Clinical Immunology
|November 1, 1996
PubMed
Summary
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Mast cells, not eosinophils, are the primary source of cysteinyl leukotrienes in aspirin-sensitive asthma. Mast cell activation explains aspirin-induced bronchoconstriction and histamine release.

Area of Science:

  • Immunology
  • Pulmonology
  • Allergy

Background:

  • Aspirin-sensitive asthma (ASA) involves cysteinyl leukotrienes (LTs), but the cellular source remains unclear.
  • Mast cells and eosinophils are implicated, with ASA patients showing increased infiltration of both cell types in bronchial biopsies.

Purpose of the Study:

  • To elucidate the cellular origin of cysteinyl leukotrienes in aspirin-sensitive asthma.
  • To differentiate the roles of mast cells and eosinophils in aspirin-induced airway hyperresponsiveness.

Main Methods:

  • Comparative analysis of bronchial biopsy samples from aspirin-sensitive and aspirin-tolerant asthma patients.
  • Assessment of serum and nasal secretion markers (histamine, tryptase, LTs) following aspirin challenge.
  • Evaluation of the effects of cromolyn sodium, nedocromil sodium, and antihistamines on aspirin- and hyperosmolar-induced bronchoconstriction.

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Main Results:

  • ASA patients exhibit greater mast cell and eosinophil infiltration, but similar eosinophil activation, compared to aspirin-tolerant controls.
  • Aspirin challenge in ASA patients elevates serum histamine and tryptase, decreases lung function, and increases nasal histamine and leukotriene C4.
  • Cromolyn sodium and nedocromil sodium prevent aspirin-induced bronchoconstriction, suggesting mast cell involvement. Antihistamines are less effective for aspirin challenge but attenuate hyperosmolar responses.

Conclusions:

  • Mast cells are the primary cellular source of cysteinyl leukotrienes driving aspirin-induced bronchoconstriction in asthma.
  • Mast cell activation, leading to histamine release, is the key mechanism in both aspirin- and hyperosmolar-induced bronchoconstriction.